東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back to Search results for [ null ]

Switch To: Labeled | MARC Mode | ISBD

The role of the dystrophin-glycoprot...

Consolino, Christina Marie.

Linked to FindBook

Google Book

Amazon

博客來

The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice./
Author:	Consolino, Christina Marie.
Description:	140 p.
Notes:	Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0489.
Contained By:	Dissertation Abstracts International64-02B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3079429
ISBN:	0496273078

The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice.
Consolino, Christina Marie.

The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice. - 140 p.

Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0489.

Thesis (Ph.D.)--University of Michigan, 2003.

The dystrophin glycoprotein complex (DGC) physically links cytoskeletal actin to the extracellular matrix (ECM) of skeletal muscle fibers, and mutations in the genes encoding many members of the DGC result in muscular dystrophy. Primary deficiencies of two proteins, dystrophin and alpha-sarcoglycan, destabilize the entire DGC in mdx and Sgca-null mice, respectively. The purpose was to examine the structure, function and susceptibility to contraction-induced injury of limb muscles of Sgca-null and mdx mice to elucidate the function of the DGC. The working hypothesis was that the DGC shunts contractile forces laterally from the myofibrils through the plasma membrane to the ECM, and deficiencies in the DGC result in a mechanically compromised cytoskeleton, increasing sarcomere heterogeneity and susceptibility to damage. Contractile and morphological properties of extensor digitorum longus (EDL) and soleus muscles of Sgca-null and wild type mice were compared, and the responses of muscles of Sgca-null and mdx mice to contraction-induced injury induced by single stretches were investigated.

ISBN: 0496273078Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice.
LDR:03439nmm 2200301 4500 001 1843024
005 20051010101550.5
008 130614s2003 eng d
020 $a 0496273078
035 $a (UnM)AAI3079429
035 $a AAI3079429
040 $a UnM $c UnM
100 1 $a Consolino, Christina Marie. $3 1931267
245 1 4 $a The role of the dystrophin-glycoprotein complex in the structure, function, and susceptibility to contraction-induced injury of limb muscles in dystrophic mice.
300 $a 140 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0489.
500 $a Chairs: Susan V. Brooks Herzog; Margaret V. Westfall.
502 $a Thesis (Ph.D.)--University of Michigan, 2003.
520 $a The dystrophin glycoprotein complex (DGC) physically links cytoskeletal actin to the extracellular matrix (ECM) of skeletal muscle fibers, and mutations in the genes encoding many members of the DGC result in muscular dystrophy. Primary deficiencies of two proteins, dystrophin and alpha-sarcoglycan, destabilize the entire DGC in mdx and Sgca-null mice, respectively. The purpose was to examine the structure, function and susceptibility to contraction-induced injury of limb muscles of Sgca-null and mdx mice to elucidate the function of the DGC. The working hypothesis was that the DGC shunts contractile forces laterally from the myofibrils through the plasma membrane to the ECM, and deficiencies in the DGC result in a mechanically compromised cytoskeleton, increasing sarcomere heterogeneity and susceptibility to damage. Contractile and morphological properties of extensor digitorum longus (EDL) and soleus muscles of Sgca-null and wild type mice were compared, and the responses of muscles of Sgca-null and mdx mice to contraction-induced injury induced by single stretches were investigated.
520 $a Compared with muscles of wild type mice, muscles of Sgca-null mice maintained 40% to 100% greater masses throughout the life span, resulting primarily from the accumulation of noncontractile material. Increases in fiber number provided some compensation for the presence of degenerating fibers in muscles of Sgca-null mice as evidenced by absolute forces and powers at or above control values. Similar forces and powers of alpha-sarcoglycan deficient and wild type muscles coupled with large masses of muscles of Sgca-null mice resulted in low specific forces and normalized powers. An exception was that soleus muscles of male Sgca-null mice employed additional, but as yet unknown, adaptations to compensate for the alpha-sarcoglycan deficiency resulting in control levels of specific force and normalized power. Compared with respective control muscles, greater force deficits were observed following single stretches of maximally activated EDL muscles of mdx mice and EDL and soleus muscles of Sgca-null mice with no indications of membrane damage. The findings are consistent with a role for the DGC in the stabilization of the alignment of sarcomeres, in addition to the previously accepted role in conferring structural support to the muscle fiber membrane.
590 $a School code: 0127.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Health Sciences, Recreation. $3 1018003
690 $a 0433
690 $a 0575
710 2 0 $a University of Michigan. $3 777416
773 0 $t Dissertation Abstracts International $g 64-02B.
790 1 0 $a Herzog, Susan V. Brooks, $e advisor
790 1 0 $a Westfall, Margaret V., $e advisor
790 $a 0127
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3079429